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Updated: Feb 11, 2026
Measuring and Altering Mating Drive in Male Drosophila melanogaster
Published on: February 15, 2017
Male-killing toxin in a bacterial symbiont of Drosophila
Toshiyuki Harumoto1, Bruno Lemaitre2
1Global Health Institute, School of Life Sciences, École Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland. toshiyuki.harumoto@epfl.ch.
Abstract:
Several lineages of symbiotic bacteria in insects selfishly manipulate host reproduction to spread in a population 1 , often by distorting host sex ratios. Spiroplasma poulsonii2,3 is a helical and motile, Gram-positive symbiotic bacterium that resides in a wide range of Drosophila species 4 . A notable feature of S. poulsonii is male killing, whereby the sons of infected female hosts are selectively killed during development1,2. Although male killing caused by S. poulsonii has been studied since the 1950s, its underlying mechanism is unknown. Here we identify an S. poulsonii protein, designated Spaid, whose expression induces male killing. Overexpression of Spaid in D. melanogaster kills males but not females, and induces massive apoptosis and neural defects, recapitulating the pathology observed in S. poulsonii-infected male embryos5-11. Our data suggest that Spaid targets the dosage compensation machinery on the male X chromosome to mediate its effects. Spaid contains ankyrin repeats and a deubiquitinase domain, which are required for its subcellular localization and activity. Moreover, we found a laboratory mutant strain of S. poulsonii with reduced male-killing ability and a large deletion in the spaid locus. Our study has uncovered a bacterial protein that affects host cellular machinery in a sex-specific way, which is likely to be the long-searched-for factor responsible for S. poulsonii-induced male killing.
Insights
Spiroplasma poulsonii bacteria manipulate insect reproduction by killing male offspring. Researchers identified a bacterial protein, Spaid, that causes this sex-specific male killing by targeting the host
Area of Science:
- Microbiology
- Genetics
- Evolutionary Biology
Background:
- Symbiotic bacteria in insects can manipulate host reproduction to enhance their own transmission.
- Spiroplasma poulsonii is a bacterium known to cause male killing in Drosophila species, but the mechanism remains elusive.
- Understanding the molecular basis of male killing is crucial for comprehending host-symbiont interactions and reproductive manipulation.
Purpose of the Study:
- To identify the specific bacterial factor responsible for Spiroplasma poulsonii-induced male killing in Drosophila.
- To elucidate the mechanism by which this factor mediates sex-specific lethality.
- To characterize the functional domains and host targets of the identified bacterial protein.
Main Methods:
- Expression of a candidate Spiroplasma poulsonii protein (Spaid) in Drosophila melanogaster to assess its effect on host survival.
- Analysis of Spaid's subcellular localization and functional domains (ankyrin repeats, deubiquitinase domain).
- Investigation of Spaid's interaction with host cellular machinery, particularly the dosage compensation complex on the male X chromosome.
- Characterization of a mutant Spiroplasma poulsonii strain with reduced male-killing ability.
Main Results:
- Overexpression of the Spaid protein in Drosophila induced male-specific lethality, apoptosis, and neural defects, mirroring natural infections.
- Spaid appears to target the dosage compensation machinery on the male X chromosome.
- Ankyrin repeats and a deubiquitinase domain within Spaid are essential for its localization and activity.
- A mutant strain lacking a functional spaid locus exhibited significantly reduced male-killing capacity.
Conclusions:
- The Spiroplasma poulsonii protein Spaid is identified as the causative agent of male killing in Drosophila.
- Spaid functions by interfering with the host's sex-specific gene expression, likely via the dosage compensation complex.
- This discovery reveals a novel bacterial mechanism for manipulating host reproduction through sex-specific targeting of host cellular processes.
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